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000138082 1001_ $$0P:(DE-2719)2810343$$aDecker, Jochen Martin$$b0$$eFirst author$$udzne
000138082 245__ $$aPro-aggregant Tau impairs mossy fiber plasticity due to structural changes and Ca(++) dysregulation.
000138082 260__ $$aLondon$$bBiomed Central$$c2015
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000138082 520__ $$aWe used an inducible mouse model expressing the Tau repeat domain with the pro-aggregant mutation ΔK280 to analyze presynaptic Tau pathology in the hippocampus.Expression of pro-aggregant Tau(RDΔ) leads to phosphorylation, aggregation and missorting of Tau in area CA3. To test presynaptic pathophysiology we used electrophysiology in the mossy fiber tract. Synaptic transmission was severely disturbed in pro-aggregant Tau(RDΔ) and Tau-knockout mice. Long-term depression of the mossy fiber tract failed in pro-aggregant Tau(RDΔ) mice. We observed an increase in bouton size, but a decline in numbers and presynaptic markers. Both pre-and postsynaptic structural deficits are preventable by inhibition of Tau(RDΔ) aggregation. Calcium imaging revealed progressive calcium dysregulation in boutons of pro-aggregant Tau(RDΔ) mice. In N2a cells we observed this even in cells without tangle load, whilst in primary hippocampal neurons transient Tau(RDΔ) expression alone caused similar Ca(++) dysregulation. Ultrastructural analysis revealed a severe depletion of synaptic vesicles pool in accordance with synaptic transmission impairments.We conclude that oligomer formation by Tau(RDΔ) causes pre- and postsynaptic structural deterioration and Ca(++) dysregulation which leads to synaptic plasticity deficits.
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000138082 650_7 $$2NLM Chemicals$$atau Proteins
000138082 650_7 $$0SY7Q814VUP$$2NLM Chemicals$$aCalcium
000138082 650_2 $$2MeSH$$aAnimals
000138082 650_2 $$2MeSH$$aCalcium: physiology
000138082 650_2 $$2MeSH$$aCalcium Signaling: physiology
000138082 650_2 $$2MeSH$$aCell Culture Techniques
000138082 650_2 $$2MeSH$$aDisease Models, Animal
000138082 650_2 $$2MeSH$$aElectrophysiology
000138082 650_2 $$2MeSH$$aHippocampus: physiology
000138082 650_2 $$2MeSH$$aLong-Term Potentiation: physiology
000138082 650_2 $$2MeSH$$aMice
000138082 650_2 $$2MeSH$$aMice, Knockout
000138082 650_2 $$2MeSH$$aMossy Fibers, Hippocampal: physiology
000138082 650_2 $$2MeSH$$aNeuronal Plasticity: physiology
000138082 650_2 $$2MeSH$$aSynaptic Transmission: physiology
000138082 650_2 $$2MeSH$$atau Proteins: deficiency
000138082 650_2 $$2MeSH$$atau Proteins: genetics
000138082 650_2 $$2MeSH$$atau Proteins: metabolism
000138082 7001_ $$0P:(DE-2719)2810335$$aKrüger, Lars$$b1$$udzne
000138082 7001_ $$0P:(DE-2719)2810788$$aSydow, Astrid$$b2$$udzne
000138082 7001_ $$aZhao, Shanting$$b3
000138082 7001_ $$aFrotscher, Michael$$b4
000138082 7001_ $$0P:(DE-2719)2541671$$aMandelkow, Eckhard$$b5$$udzne
000138082 7001_ $$0P:(DE-2719)2541658$$aMandelkow, Eva-Maria$$b6$$eLast author$$udzne
000138082 77318 $$2Crossref$$3journal-article$$a10.1186/s40478-015-0193-3$$b : Springer Science and Business Media LLC, 2015-04-03$$n1$$p23$$tActa Neuropathologica Communications$$v3$$x2051-5960$$y2015
000138082 773__ $$0PERI:(DE-600)2715589-4$$a10.1186/s40478-015-0193-3$$gVol. 3, no. 1, p. 23$$n1$$p23$$q3:1<23$$tActa Neuropathologica Communications$$v3$$x2051-5960$$y2015
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